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Biomedical subjects

C Pastor

Publications and source records attributed to C Pastor.

At least 55 records · Page 3Linked to original sources
PubMed1995

Conventional viral cultures and shell vial assay for diagnosis of apparently culture-negative Coxiella burnetii endocarditis.

A patient with culture-negative endocarditis was diagnosed with Q fever endocarditis based on the results of serological tests and positive leukocyte cultures obtained using conventional viral cultures and the shell vial technique. This case report suggests that isolation of Coxiella burnetii from blood may allow better diagnostic and therapeutical evaluation of patients with Q fever endocarditis. The use of both conventional and shell vial viral cultures is recommended for the isolation of Coxiella burnetii from the blood of patients with apparently culture-negative endocarditis.

Adult↗
PubMed1995

Involvement of different types of voltage-sensitive calcium channels in the presynaptic regulation of noradrenaline release in rat brain cortex and hippocampus.

Transmitter release at the nerve terminal is mediated by the influx of Ca2+ through voltage-sensitive calcium channels (VSCCs). Many types of VSCCs have been found in neurons (T, N, L, and P), but uncertainty remains about which ones are involved in neuronal excitation-secretion coupling. Specific ligands for the L- and N-type VSCCs were used to determine which of these subtypes might be involved in the K(+)-evoked [3H]noradrenaline release from superfused rat brain cortical and hippocampal synaptosomes. In cortical presynaptic terminals the 1,4-dihydropyridine agonist Bay K8644 enhanced the K+ (15 mM)-evoked [3H]noradrenaline release. This effect was reversed by the 1,4-dihydropyridine antagonists nimodipine and nitrendipine. The L-type VSCC ligands had no effect on hippocampal synaptosomes. In contrast, the N-type VSCC blocker omega-conotoxin markedly reduced the K(+)-evoked [3H]noradrenaline release in nerve terminals from both regions. Inhibition was greater in hippocampal synaptosomes. When applied together the inhibitory actions of nimodipine and omega-conotoxin were approximately additive. These findings indicate that both L- and N-type VSCCs participate in noradrenaline release in rat brain cortex and suggest that noradrenergic terminals in the two regions examined may have distinct populations of VSCCs: L type in cortex and N type in hippocampus.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1994

Differential contribution of L- and N-type calcium channels on rat hippocampal acetylcholine release.

Bay K 8644, nimodipine and omega-conotoxin GVIA (omega-CgTx) were used to study the different contribution of voltage-sensitive calcium channels (VSCC) to [3H]acetylcholine ([[3H]ACh) release in rat hippocampal synaptosomes. In our experimental conditions, the percentage of calcium-dependent ACh release was approximately 80%. Nimodipine (0.01-10 microM) and Bay 8644 (0.01-10 microM) were not able to modify the [3H]ACh release under stimulating conditions (15 mM K+). Nevertheless, when K+ concentration was reduced to 8 mM, a significant increase in [3H]ACh release was observed at 1 and 10 microM of Bay K 8644. Nimodipine (0.01-10 microM) failed to reverse the effect of Bay K 8644 on [3H]ACh release. Finally, omega-CgTx (0.001-1 microM) caused a concentration-dependent reduction of [3H]ACh release in K+ (15 mM)-stimulating conditions. These results suggest that the N-type VSCC probably play a predominant role in regulating the [3H]ACh release in synaptosomes from rat hippocampus.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1994

Effects of L-arginine and L-nitro-arginine treatment on blood pressure and cardiac output in a rabbit endotoxin shock model.

OBJECTIVE: To verify the effect of nitric oxide system modification during sepsis, not only in terms of pressure but also in terms of perfusion flow. DESIGN: Experimental, comparative study. SETTING: Laboratory of a university hospital. SUBJECTS: Twenty-six New Zealand male rabbits (2 to 2.5 kg body weight) were studied under anesthesia. INTERVENTIONS: Nitric oxide pathways were modified during shock-induced hypotension, using L-arginine (600 mg/kg) and L-nitro-arginine (7.5 mg/kg), which were infused 75 mins after endotoxin injection. MEASUREMENTS AND MAIN RESULTS: Mean arterial pressure (MAP) and cardiac output, as well as ascending aortic velocity, were measured and aortic conductance (aortic velocity/MAP in cm/sec/mm Hg) was calculated. Both L-arginine and L-nitro-arginine increased MAP to the pre-endotoxin level, but only L-arginine increased aortic velocity in association with a marked increase in aortic conductance (p < .001). L-nitro-arginine significantly (p < .05) decreased aortic velocity as compared with the control endotoxin group, with an intense vasoconstriction as shown by a significant (p < .001) decrease in aortic conductance. CONCLUSIONS: These results, along with the high mortality rate in the L-nitro-arginine treated group, challenge the hypothesis that nitric oxide release inhibition has a beneficial effect in septic shock.

Animals↗